Host-associated reservoirs account for the majority of recurrent and oftentimes recalcitrant infections. Previous studies established that uropathogenic E. colithe primary cause of urinary tract infections (UTIs)can adhere to vaginal epithelial cells preceding UTI. Here, we demonstrate that diverse urinary E. coli isolates not only adhere to, but also invade vaginal cells. Intracellular colonization of the vaginal epithelium is detected in acute and chronic murine UTI models indicating the ability of E. coli to reside in the vagina following UTI. Conversely, in a vaginal colonization model, E. coli are detected inside vaginal cells and the urinary tract, indicating that vaginal colonization can seed the bladder. More critically, bacteria are identified inside vaginal cells from clinical samples from women with a history of recurrent UTI. These findings suggest that E. coli can establish a vaginal intracellular reservoir, where it may reside safely from extracellular stressors prior to causing an ascending infection.
Blue light irradiation (BLI) is an FDA‐approved method for treating certain types of infections, like acne, and is becoming increasingly attractive as an antimicrobial strategy as the prevalence of antibiotic‐resistant “superbugs” rises. However, no study has delineated the effectiveness of BLI throughout different bacterial growth phases, especially in more BLI‐tolerant organisms such as Escherichia coli. While the vast majority of E. coli strains are nonpathogenic, several E. coli pathotypes exist that cause infection within and outside the gastrointestinal tract. Here, we compared the response of E. coli strains from five phylogenetic groups to BLI with a 455 nm wavelength (BLI 455), using colony‐forming unit and ATP measurement assays. Our results revealed that BLI 455 is not bactericidal, but can retard E. coli growth in a manner that is dependent on culture age and strain background. This observation is critical, given that bacteria on and within mammalian hosts are found in different phases of growth.
Sensory systems allow pathogens to differentiate between different niches and respond to stimuli within them. A major mechanism through which bacteria sense and respond to stimuli in their surroundings is two-component systems (TCSs). TCSs allow for the detection of multiple stimuli to lead to a highly controlled and rapid change in gene expression. Here, we provide a comprehensive list of TCSs important for the pathogenesis of uropathogenic Escherichia coli (UPEC). UPEC accounts for >75% of urinary tract infections (UTIs) worldwide. UTIs are most prevalent among people assigned female at birth, with the vagina becoming colonized by UPEC in addition to the gut and the bladder. In the bladder, adherence to the urothelium triggers E. coli invasion of bladder cells and an intracellular pathogenic cascade. Intracellular E. coli are safely hidden from host neutrophils, competition from the microbiota, and antibiotics that kill extracellular E. coli. To survive in these intimately connected, yet physiologically diverse niches E. coli must rapidly coordinate metabolic and virulence systems in response to the distinct stimuli encountered in each environment. We hypothesized that specific TCSs allow UPEC to sense these diverse environments encountered during infection with built-in redundant safeguards. Here, we created a library of isogenic TCS deletion mutants that we leveraged to map distinct TCS contributions to infection. We identify – for the first time – a comprehensive panel of UPEC TCSs that are critical for infection of the genitourinary tract and report that the TCSs mediating colonization of the bladder, kidneys, or vagina are distinct.
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